Since PPARα has been known to activate fatty acid oxidation (FAO) and to decrease glucose utilization [17], we hypothesized that PPARα antagonism might cause the cells to decrease their reliance on FAO and thus be exquisitely dependent on glycolysis for their energy source; such a finding would suggest a novel approach for clinical utility of PPARα antagonists, especially with regard to RCC therapy. This evidence concerns the gene PPARA and renal cell carcinoma.